Background:Prior data on iron deficiency anemia’s (IDA) prevalence and associated risk factors among female university students are scarce in the Saudi Arabian context. This study therefore recruited a sample of female students at the University of Tabuk, Saudi Arabia, to investigate IDA prevalence and risk factors and fill the identified research gap.Methods:A cross-sectional study of 200 apparently healthy female students aged between 19 and 25 years was performed between February and June 2016. Data on the participants’ sociodemographics, diet, health, anthropometry, and hematological and biochemical iron status indices were gathered. A logistic regression analysis then revealed the IDA risk factors.Results:The IDA prevalence was 12.5%. The factors associated via logistic regression with an elevated anemia risk were inadequate iron and vitamin C intakes, infrequent (≤2 times per week) consumption of red meat, frequent (≥2 times per week) tea consumption, and a past personal history of IDA.Conclusions:The findings suggest that focused education and awareness strategies are needed to improve nutritional habits by encouraging the consumption of rich dietary iron sources and by raising awareness of the food and drinks which facilitate or hinder the bioavailability of iron.
Background BRCA1/2 pathogenic variants have become associated with familial breast and ovarian cancers, and hereditary cancer‐predisposition syndrome. With advances in molecular biology, BRCA profiling facilitates early diagnosis and the implementation of preventive and therapeutic strategies. The genes exhibit variable prevalence among different individuals and moderate interpretation complexity. BRCA deficiency is instrumental in cancer development, affects therapeutic options and is instrumental in drug resistance. In addition, BRCA1/2 profile is diverse across different groups and has been associated with the “founder effect” in certain populations. Methods In this review, we aim to detail the spectrum of BRCA1/2 variants and their associated risk estimates. Results The relationship between BRCA1/2 and hereditary and familial cancers is indisputable, yet BRCA screening methods are beset with limitations and lack clinical confidence. Conclusion This review emphasizes the importance of screening BRCA genetics, in addition to their clinical utility. Furthermore, founder variants are anticipated in the Saudi population.
Purpose Selenium nanoparticles (SeNPs) have recently gained much attention in nanomedicine applications owing to their unique biological properties. Biosynthesis of SeNPs using nutraceuticals as lycopene (LYC) maximizes their stability and bioactivities. In this context, this study aimed to elucidate the renoprotective activity of SeNPs coated with LYC (LYC-SeNPs) in the acute kidney injury (AKI) model. Methods Rats were divided into six groups: control, AKI (glycerol-treated), AKI+sodium selenite (Na 2 SeO 3 ; 0.5 mg/kg), AKI+LYC (10 mg/kg), AKI+LYC-SeNPs (0.5 mg/kg) and treated for 14 days. Results Glycerol treatment evoked significant increases in rhabdomyolysis-related markers (creatine kinase and LDH). Furthermore, relative kidney weight, Kim-1, neutrophil gelatinase-associated lipocalin (NGAL), serum urea, and creatinine in the AKI group were elevated. Glycerol-injected rats displayed declines in reduced glutathione level, and superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase activities, paralleled with downregulations in Nfe2l2 and Hmox-1 expressions and high renal MDA and NO contents. Glycerol-induced renal inflammation was evident by rises in TNF-α, IL-1β, IL-6, and upregulated Nos2 expression. Also, apoptotic (elevated caspase-3, Bax, and cytochrome-c with lowered Bcl-2) and necroptotic (elevated Pipk3 expression) changes were reported in damaged renal tissue. Co-treatment with Na 2 SeO 3 , LYC, or LYC-SeNPs restored the biochemical, molecular, and histological alterations in AKI. In comparison with Na 2 SeO 3 or LYC treatment, LYC-SeNPs had the best nephroprotective profile. Conclusion Our findings authentically revealed that LYC-SeNPs co-administration could be a prospective candidate against AKI-mediated renal damage via antioxidant, anti-inflammatory, anti-apoptotic and anti-necroptotic activities.
Thrombin is a multifunctional serine protease generated in injured cells. The generation of thrombin in coagulation plays a central role in the functioning of haemostasis. The last enzyme in the coagulation cascade is thrombin, with the function of cleaving fibrinogen to fibrin, which forms the fibrin clot of a haemostatic plug. Although thrombin primarily converts fibrinogen to fibrin, it also has many other positive regulatory effects on coagulation. Thrombin has procoagulant, inflammatory, cellular proliferation and anticoagulant effects. In coagulation system, thrombin has two very distinct roles. Firstly, it acts as a procoagulant when it converts fibrinogen into an insoluble fibrin clot, activates factor (F) XIII, activates thrombin activatable fibrinolysis inhibitor (TAFI) and activates FV, FVIII and FXI. Thrombin also enhances platelet adhesion by inactivating a disintegrin and metalloprotease with thrombospondin type1 motif (ADAMTS13). However, when thrombin activates protein C, it acts as an anticoagulant. A natural anticoagulant pathway that supplies regulation of the blood coagulation system contains protein C, which is the key component. This is accomplished by the specific proteolytic inactivation of FV and FVIII. In this review, the multiple roles of thrombin in the haemostatic response to injury are studied in addition to the cofactors that determine thrombin activity and how thrombin activity is thought to be coordinated.
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